Development of methods to promote degradation of amyloid beta

老年斑是阿尔茨海默病的病理标志。主要成分是淀粉样蛋白β 42（Aβ42）。抑制Aβ42的生成或增强Aβ42的降解是开发治疗AD方法的基本途径。我们发现，BACE，脱落β-淀粉样蛋白前体（βAPP）产生CTF-β，在两个位点切割Aβ42成为毒性和疏水性小得多的物种。我们还研究了Aβ42的产生机制。

Senile plaque is a pathological hallmark of Alzheimer's disease. The major component is amyloid-beta 42 (Aβ42). Inhibition of Aβ42 generation or enhancement of Aβ42 degradation is fundamental approach in developing methods to treat AD. We found that BACE, which sheds beta-amyloid protein precursor (βAPP) to generate CTF-β, cleaves Aβ42 at two sites into species with much less toxicity and hydrophobicity. We also investigated the generation mechanism of Aβ42.